The goal of the proposed research is to elucidate the neural mechanisms in the spinal cord that underlie the generation of rhythmic locomotory output and to determine, at the cellular level, the role of putative amino acid transmitters in the production and control of spinal locomotion. The study will be done on an in vitro lamprey spinal cord preparation that generates "fictive locomotion", the neuronal correlate of locomotory behavior. The first objective of the proposed study is to identify and describe the interneurons or types of interneurons that may be a part of the locomotory central pattern generator, those neurons with membrane potential oscillations and/or spike activity correlated with the pattern of efferent discharge. The description of each neuron will include physiological properties and morphological characteristics, as revealed by intracellular dye injection. Evidence of synaptic connections between the neuron being characterized and other components of the spinal cord will be gathered and tests to determine the role each neuron plays in the network will be performed. Amino acid transmitter receptor agonists and antagonists have powerful effects on the locomotory motor output generated by the spinal cord. The second objective of the proposed research is to determine the effects of amino acid neurotransmitter receptor agonists and antagonists on the central pattern generator by combining a study of the effects of these pharmacological agents on the activity of individual interneurons during fictive locomotion with a detailed description of each recorded neuron's physiological and morphological characteristics. The results of this study can provide insights into how the spinal network is organized and at what level in the organization of the network these agents operate. Furthermore, any agents found to act specifically to turn on or modulate spinal centers for locomotion may be related to transmitter than function in the control of locomotion by descending systems from the brain, control that is lost following spinal transection.